Narrowing of the opening surface of the mitral valve causing a gradient of diastolic pressure between the atrium and the left ventricle. Mitral stenosis is defined as the reduction of the mitral valvular orifice of the heart, sometimes caused by an inflammatory process that affects the valvular flaps or their supporting apparatus, sometimes by degenerative processes, such as calcification of the annulus linked to the age. This causes an obstacle to the passage of blood from the left atrium to the left ventricle. It can be, although in a few cases, also of congenital origin.
The most frequent: rheumatic fever (with rheumatic endocarditis). More rarely, endocarditis of bacterial origin. Rarely: stenosis of the mitral valve of functional origin caused by diastolic prolapse of atrial tumors (eg, myxoma) in the mitral valve region. The cause of mitral stenosis was usually rheumatic in pre-antibiotic era. Group A streptococci (cf. rheumatic fever) have surface antigens structurally similar to some proteins present in the valvular structure; the resulting antigen-antibody reaction causes the formation of numerous small fibrotic nodules on the valvular flaps, which over time undergo calcification and retraction. The process can extend to the tendon cords, which represent the mechanical support of the valves, causing their fibrotic stiffening, with consequent stopping the movement of the valvular flaps, which, once calcified, give the valve the "fish mouth" appearance.
Consequences of increased pressure and enlargement of the left atrium:
- often absolute arrhythmia with atrial fibrillation;
- arterial embolism in the presence of atrial thrombus: cerebral ischemic attack,
occlusion of peripheral arteries, embolism of the renal arteries, mesenteric
infarct.
Consequences of left heart failure:
- decrease in performance, dyspnea under stress and at rest, nocturnal cough
- gasps from congestion above the lungs, sputum to red coloration.
Consequences of right (secondary) heart failure:
- jugular vein congestion, edema, congestive liver, proteinuria.
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Facies mitralis: reddened cheeks.
Auscultation: 3rd tympanic heart tone, mitral opening tone followed by decreasing diastolic murmur with maximum point above the apex of the heart, murmur in presystolic crescendo in sinus rhythm. The cardiac objectivity varies according to the severity of the lesion. At palpation, the toe of the tip is perceived in normal. In the precordial site a diastolic thrill is perceptible, determined by the vortices generated by the passage of blood through the stenotic valve. The most useful findings for diagnostic purposes are obtained with auscultation, and are more easily audible at the mitral focus and with the patient in left lateral decubitus. The first tone has accentuated intensity and reduced duration. The systolic pause is completely free. The second tone is only increased when pulmonary arterial hypertension develops. In protodiastole we can feel an added tone (at 0.04-0.12 sec from the aortic component of the second tone), the so-called snap or opening tone of the mitral, characterized by short duration and high frequency. The more severe the stenosis, the more the pop will be premature. Subsequently, a low-frequency breath (diastolic roll) begins which has a duration proportional to the severity of the stenosis.
| Classification of the degree of severity based on the average pressure gradient above the valve and the valve opening surface | ||
| Degree of gravity | Medium gradient in mmHg |
Surface of opening valvular |
| mild | <7 | 1.2-2.5 cm2 |
| medium | 8-15 | 1-1.5 cm2 |
| severe | > 15 | <1 cm2 |
ECG
sinus rhythm with absolute P-arrhythmia arrhythmia, with atrial
fibrillation, from vertical position to deviation of the right axis, sign of
right overload.
Chest radiography: sometimes calcification of the valve and the mitral ring,
mitral heart with groove formation and lateral visible narrowing of the
retrocardial space (enlarged left atrium) and of the retrosternal space (with
hypertrophy of the right heart), protruding pulmonary segment, pulmonary
congestion .
Echocardiography
- B-Mode: thickening / calcification of the mitral cusp, "diastolic dome" of the
mitral cusp, enlargement of the left atrium, atrial thrombus ?, quantification
of the stenosis in the short parasternal axis with planimetry of the opening
surfaces.
- M-Mode: reduction of the ejection factor, model M raised, concordant movement
of the posterior valve cusp.
- Doppler: quantification of the stenosis through examination of the valve
opening surface, e.g. according to the pressure-half-time method.
Cardiac catheterization
- right heart catheterization: higher pressure values in the pulmonary
circulation and then also in the right heart, determination of the volume of the
heart in the unit of time
- left cardiac catheterization: determination of the diastolic pressure gradient
between atrium and left ventricle and of the valve opening surface. Evident
concomitant insufficiency of the mitral valve or other defects of the heart
valves, AC
Pharmacological therapy:
- therapy of heart failure with diuretics, ineffective ACE inhibitors
- digital therapy and anticoagulants with protracted action.
Surgical therapy starting from stage III NYHA:
- percutaneous opening of the mitral valve with balloon catheter (= balloon
valvuloplasty)
- valve reconstruction in the presence of sufficient mobility of the valvular
cusps
- valve replacement.
Surgery of valvuloplasty, commissurotomy, valvular repair or valve replacement
is necessary before the presence of stenosis becomes severe and, associated with
atrial fibrillation, causes a severe decline in cardiac function. The
commissurotomy can only be performed if the flaps are not calcified and the
subvalvular apparatus is preserved. Via a left anterior thoracotomy, the chest
is accessed through the resection space of the V coast. When the pericardium is
opened through the left auricle, a diverter is introduced into the mitral atria,
which, by opening, forces the valvular flaps to separate the merged commissures.
Mitral valve replacement provides a left antero-lateral thoracotomy with
sub-periosteal excision of the V-rib; the patient is placed in extracorporeal
circulation (CEC). The valve is replaced with a measuring prosthesis congruous
to the natural annulus. Survival rate at 5 years without intervention in the
presence of an average stenosis about 60%. with severe stenosis about 10%,
following timely valvuloplasty about 80 ".